We propose a study of unmedicated schizophrenic patients utilizing the new non-invasive neurophysiological topographic technique of brain electrical activity mapping (BEAM). We will combine this with assessment of cognitive functions with the thought disorder index (TDI) and clinical assessment scales to measure negative and positive symtoms and clinical status. We believe that the simultaneous, quantitative assessment of neurophysiological, cognitive and clinical variables is essential to understanding which neurophysiological signs are correlated with which clinical variables and form natural subgroups of the schizophrenia syndrome. Important methodological features of the study include the use of a matched normal control group and an unmedicated comparison group of affective disorder psychotic patients to determine which neurophysiological variables may differentiate schizophrenics from affective disorders psychosis. All patients will be off medication for a minimum of 14 days. Furthermore, this study will clarify and extend our earlier BEAM findings in medicated patients: (1) A deficiency in integrated left temporal amplitude of auditory P300 topography in the schizophrenic group and which also correctly diagnosed 9/10 individual schizophrenics and 9/10 normals; (2) Increased frontal slowing (delta) in the spectral energy topography of the schizophrenic group. In the study proposed we will determine if the above BEAM findings can be used, in a new and unmedicated group, to differentiate schizophrenics from normals and from affective disorder patients with psychosis, using controls for motivational and attentional factors. We will determine if the following findings are positively correlated and form a natural schizophrenic subgroup: deficits in the P300 left temporal amplitude feature increased looseness, bizarreness, and related categories in the TDI; and increased positive clinical symptoms of hallucinations and delusions. We will determine if another natural schizophrenic subgroup is characterized by increased frontal EEG slowing (delta); structural evidence of diffuse brain pathology (increased CSF spaces); neuropsychological test deficits associated with frontal lobe pathology; poverty of output and a lesser degree of bizarreness on the TKI; and increased negative clinical symptoms.